Примери за използване на Replicons на Английски и техните преводи на Български
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Stable replicons.
Replicons containing NS5B from clinical.
NS5A transient replicons.
Replicons containing NS5A from clinical.
Data obtained from transiently transfected replicons.
Replicons containing NS5B from clinical isolates.
Table 6: Activity of ledipasvir andsofosbuvir against chimeric replicons.
Replicons containing NS5A from clinical isolates.
Activity of sofosbuvir and velpatasvir against full-length orchimeric laboratory replicons.
Replicons containing NS3 protease from clinical isolates.
Activity of sofosbuvir andvelpatasvir against transient replicons containing NS5A or NS5B from clinical isolates.
Transient replicons carrying NS5A or NS5B from patient isolates.
Amino acid substitutions in NS3 or NS5A selected in cell culture orimportant for the inhibitor class were phenotypically characterized in replicons.
B Stable chimeric 1b replicons carrying NS5B genes from genotype 2b, 5a or 6a were used for testing.
The presence of 40% human serum had no effect on the anti-HCVactivity of sofosbuvir but reduced the anti-HCV activity of velpatasvir by 13-fold against genotype 1a HCV replicons.
In genotype 1b replicons, single NS5A substitutions L31F and Y93H reduced elbasvir antiviral activity by 17-fold.
EC50 values of glecaprevir andpibrentasvir against chimeric replicons encoding NS3 or NS5A from clinical isolates are presented in Table 6.
In genotype 4 replicons, single NS5A substitutions L30S, M31V, and Y93H reduced elbasvir antiviral activity by 3to 23-fold.
Activity of sofosbuvir, velpatasvir andvoxilaprevir against transient replicons containing NS5A, NS5B or NS3 protease from clinical isolates.
In genotype 1b replicons, single NS3 substitutions F43S, A156S/T/V, and D168A/G/V reduced grazoprevir antiviral activity by 3- to 375-fold.
For sofosbuvir, the NS5B substitution S282T was selected in genotype 1-6 replicons and was associated with 2- to 18-fold reduced susceptibility to sofosbuvir.
HCV replicons expressing the sofosbuvir-associated resistance substitution S282T were fully susceptible to other classes of anti-HCV agents.
The EC50 values of glecaprevir and pibrentasvir against full-length or chimeric replicons encoding NS3 or NS5A from laboratory strains are presented in Table 5.
The presence of 40% human serum had no effect on the anti-HCV activity of sofosbuvir but reduced the anti-HCV activity of velpatasvir and voxilaprevir by 13- and 6.8-fold, respectively,against genotype 1a HCV replicons.
For velpatasvir in genotype 1-6 replicons, resistance-associated substitutions selected in 2 or more genotypes were L31I/V and Y93H.
Additionally, resistance to simeprevir was evaluated in HCV genotype 1a and1b replicon assays using site-directed mutants and chimeric replicons carrying NS3 sequences derived from clinical isolates.
For voxilaprevir in genotype 1-6 replicons, resistance-associated substitutions selected in 2 or more genotypes were Q41H, A156V/T/L and D168E/H/Y.
The EC50 values of ledipasvir and sofosbuvir against full-length or chimeric replicons encoding NS5A and NS5B sequences from clinical isolates are detailed in Table 7.
Ninety-six percent of simeprevir-selected genotype 1 replicons carried one or multiple amino acid substitutions at NS3 protease positions 43, 80, 155, 156, and/or 168, with substitutions at NS3 position D168 being most frequently observed(78%).
The 50% effective concentration(EC50) values of sofosbuvir andvelpatasvir against full-length or chimeric replicons encoding NS5B and NS5A sequences from the laboratory strains are presented in Table 4.